ArticleFrontiers in oncology2026
ADGRD1 promotes bladder cancer progression and angiogenesis via the PI3K/AKT/mTOR-mediated pro-angiogenic secretome.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Bladder cancer (BLCA) remains a major cause of cancer-related mortality, particularly in advanced and metastatic stages. Identifying molecular drivers of tumor aggressiveness is critical for developing targeted therapies. Adhesion G protein-coupled receptor D1 (ADGRD1, also known as GPR133) is an orphan aGPCR recently implicated in tumorigenesis. However, its role in bladder cancer and underlying signaling mechanisms remain unknown. Methods: The clinical significance of ADGRD1 was analyzed using GEPIA3 datasets, focusing on clinical stage and prognosis. Stable ADGRD1-knockdown and overexpression BLCA cell lines were established. qPCR, Western blot, CCK-8, colony formation, wound-healing, Transwell, and HUVEC tube formation assays were used to assess proliferation, migration, invasion, and angiogenesis. Xenograft models were used to evaluate Results: ADGRD1 expression was significantly enriched in advanced-stage and high-grade BLCA, where it serves as a robust predictor of poor overall survival and progression-free interval. Functional assays demonstrated that ADGRD1 promotes BLCA cell proliferation, migration, invasion, and endothelial tube formation Conclusions: This study identifies ADGRD1 as a key progression-associated driver in BLCA. By modulating the PI3K/AKT/mTOR signaling axis and the pro-angiogenic microenvironment, ADGRD1 facilitates tumor growth and neovascularization. ADGRD1 may serve as a promising prognostic biomarker and therapeutic target for advanced BLCA.
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